Cognitive Dysfunction and Antiphospholipid Antibodies

Appenzeller, Simone; Lapa, Aline Tamires; Carvalho, Jozélio Freire de; Peres, Fernando Augusto; Shoenfeld, Yehuda

doi:10.1007/s11926-011-0224-4

Cited by 11 publications

(3 citation statements)

References 20 publications

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“…This finding suggests that aPL may act determining not only a focal damage (at level of thrombotic event), but also a more diffuse damage, with a direct mechanism on neural cells. [ 41 , 42 ] Moreover, disease activity and chronic damage seem to influence CI. Interestingly, the presence of flares assessed according with SLEDAI-2K modifications, resulted significantly associated with a worsening in the memory domain.…”

Section: Discussionmentioning

confidence: 99%

Cognitive dysfunction improves in systemic lupus erythematosus: Results of a 10 years prospective study

et al. 2018

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ObjectiveCognitive impairment (CI) has been described in 3–80% of Systemic lupus erythematosus (SLE) patients but only short-term studies evaluated its over-time changes, suggesting that CI is usually a stable finding. We aimed at evaluating the changes of SLE-related CI in a 10-years prospective single center cohort study.MethodsWe evaluated 43 patients (M/F 5/38; mean age = 45.7±10.1 years; mean disease duration = 230.8±74.3 months) at baseline (T0) and after 10 years (T1). A test battery designed to detect fronto-subcortical dysfunction across five domains (memory, attention, abstract reasoning, executive and visuospatial function) was administered. A global cognitive dysfunction score (GCD) was obtained and associated with clinical and laboratory features.ResultsPrevalence of CI was 20.9% at T0 and 13.9% at T1 (P = NS). This impairment was prevalently mild at T0 (55.5%) and mild or moderate at T1 (36.3% for both degrees). After 10 years, CI improved in 50% of patients, while 10% worsened. Impaired memory (P = 0.02), executive functions (P = 0.02) and abstract reasoning (P = 0.03) were associated with dyslipidemia at T0. Worsening of visuospatial functions was significantly associated with dyslipidemia and Lupus Anticoagulant (P = 0.04 for both parameters). Finally, GCD significantly correlated with chronic damage measured by SLICC/damage index at T0 (r = 0.3; P = 0.04) and T1 (r = 0.3; P = 0.03).ConclusionsFor the first time, we assessed CI changes over 10-years in SLE. CI improved in the majority of the patients. Furthermore, we observed an improvement of the overall cognitive functions. These results could suggest that an appropriate management of the disease during the follow-up could be able to control SLE-related CI.

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Section: Discussionmentioning

confidence: 99%

Cognitive dysfunction improves in systemic lupus erythematosus: Results of a 10 years prospective study

et al. 2018

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“…Furthermore, the intracerebroventricular injection of aPL antibodies from APS patients directly into mouse brains caused impairment in cognitive performance and the onset of hyperactive behavior [ 42 ]. The microscopic examination of brain tissue in mouse models of APS with cognitive impairment revealed a mononuclear inflammatory infiltrate in the choroid plexus and the hippocampus without evidence of ischemic lesions [ 41 , 43 , 44 , 45 ]. In vitro studies also showed that aPL antibodies bind to central nervous system neuronal cells [ 42 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Cognitive Impairment in Anti-Phospholipid Syndrome and Anti-Phospholipid Antibody Carriers

et al. 2022

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Cognitive impairment is frequently reported among anti-phospholipid syndrome (APS) patients as well as anti-phospholipid antibody (aPL) carriers, but it is less studied than other manifestations of this condition. Moreover, the exact prevalence of cognitive impairment in these patients has not been accurately determined, mainly due to inconsistency in the tools used to identify impairment, small sample sizes, and variability in the anti-phospholipid antibodies measured and positivity cutoffs. The notion of a direct pathogenic effect is supported by the observation that the higher the number of aPLs present and the higher the load of the specific antibody, the greater the risk of cognitive impairment. There is some evidence to suggest that besides the thrombotic process, inflammation-related pathways play a role in the pathogenesis of cognitive impairment in APS. The cornerstone treatments of APS are anti-coagulant and anti-thrombotic medications. These treatments have shown some favorable effects in reversing cognitive impairment, but solid evidence for the efficacy and safety of these treatments in the context of cognitive impairment is still lacking. In this article, we review the current knowledge regarding the epidemiology, pathophysiology, clinical associations, and treatment of cognitive impairment associated with APS and aPL positivity.

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“…The pathogenesis of aPL-mediated dementia in APS is not entirely understood. Suggested mechanisms include aPLs-induced BBB disruption ( Katzav et al, 2010 ), aPLs-related microvascular thrombosis ( Asherson et al, 1987 ; Denburg et al, 1997 ), or a direct effect of aPLs on brain tissues ( Appenzeller et al, 2012 ). Thrombotic events triggered by aPL might contribute to the multiple cerebral thrombotic symptoms and greater aggression to the brain ( de Godoy et al, 2000 ).…”

Section: Introductionmentioning

confidence: 99%

Presence of Anticardiolipin Antibodies in Patients with Dementia: A Systematic Review and Meta-Analysis

Islam

Alam

Kamal

et al. 2017

Front. Aging Neurosci.

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Growing evidences are supporting towards the involvement of antiphospholipid antibodies [aPLs e.g., lupus anticoagulant (LA), anticardiolipin (aCL) and anti-β2-glycoprotein I (anti-β2-GPI) antibodies] in various neurological manifestations including migraine, epilepsy and dementia in the presence or absence of autoimmune diseases such as antiphospholipid syndrome or systemic lupus erythematosus. The aim of this systematic review and meta-analysis was to assess the presence of aPLs in dementia patients without a diagnosis of any autoimmune disease. Electronic databases (e.g., PubMed, Web of Science, Scopus, ScienceDirect and Google Scholar) were searched without any year or language restrictions and based on the inclusion criteria, nine prospective case-control studies assessing only aCL were included involving 372 dementia patients and 337 healthy controls. No studies were found to assess the presence of both LA or anti-β2-GPI. The study-specific odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects model. We observed the prevalence of aCL in dementia was higher (32.80%) than that of controls (9.50%) e.g., 3.45 times higher risk of presenting with dementia than the controls, and significant presence of aCL antibodies was detected in dementia patients compared to controls (OR: 4.94, 95% CI: 2.66 – 9.16, p < 0.00001; I2 = 32%, p = 0.16). Publication bias was not observed from Egger’s (p = 0.081) and Begg’s tests (p = 0.180). Based on the study quality assessment using modified Newcastle–Ottawa Scale for case-control studies, seven of nine studies were of high methodological quality scoring ≥ 7 (median value). In summary, aCL antibodies were significantly present in dementia patients suggesting that aCL antibodies are generated due to the autoimmune-derived effects of dementia or there might be a potential causative role of this autoantibody in dementia pathogenesis.

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Cognitive Dysfunction and Antiphospholipid Antibodies

Cited by 11 publications

References 20 publications

Cognitive dysfunction improves in systemic lupus erythematosus: Results of a 10 years prospective study

Cognitive dysfunction improves in systemic lupus erythematosus: Results of a 10 years prospective study

Cognitive Impairment in Anti-Phospholipid Syndrome and Anti-Phospholipid Antibody Carriers

Presence of Anticardiolipin Antibodies in Patients with Dementia: A Systematic Review and Meta-Analysis

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